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B1 > Protein Trafficking > Flashcards

Protein Trafficking Flashcards

1
Q

Which of the following pathways does not utilize vesicular transport

a) Golgi –> ER
b) secretory vesicles –> cell exterior
c) lysosome to late endosome
d) nucleus to cytosol

A

d) gated transport

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2
Q

What are the two ways that a signal can be built into a protein?

A

1) signal sequence (continuous linear sequence)

2) signal patch (3D conformation of signal sequence)

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3
Q

What three types of nucleoporins are found in NPC?

A 
TM ring proteins (anchor NPC to envelope)
scaffold nucleoporins (form layered ring structures)
channel nucleoporins (line central pore)
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4
Q

How do the receptor-like fibrils that protrude from NPC differ?

A

On nuclear side, converge to form basket like structure

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5
Q

What size of molecules diffuse into nucleus freely via aqueous pores?

A

5kDa or less

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6
Q

What size proteins cannot enter nucleus via passive diffuse

A

50kDa and above

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7
Q

Describe the role of Ran in nuclear import

A

In nucleus, Ran-GTP binds to import receptor and cargo is released.
Once import receptor back in nucleus, Ran-GAP dephosphorylates Ran-GTP and it dissociates.
Import receptor can pick up cargo again.

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8
Q

Describe the role of Ran in nuclear export

A

Ran-GTP promotes cargo binding to export receptor

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9
Q

What is NFAT?

A

nuclear factor of activated T-cells

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10
Q

Describe the cycle of NFAT during T cell activation

A
  • T cell activation causes high calcium in active T cell.
  • Calcineurin binds and dephosphorylates NFAT, exposing its nuclear import signal.
  • NFAT imported, activates IL-2 gene transcription.
  • Ca++ eventually decreases
  • Calcineurin drops off and NFAT is phosphorylated (using ATP) exposing nuclear export signal
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11
Q

What is the role of IL-2?

A

Stimulates clonal expansion of memory T cells

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12
Q

How does cyclosporine work to prevent organ rejection?

A

Inhibits calcineurin, prevents phosphorylation of NFAT and therefore NFAT translocation into T cells

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13
Q

What occurs to collagen polypeptide after translation? (up until ER)

A

Signal sequence on polypeptide is targeted to ER by signal recognition particle

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14
Q

Describe co-translational translocation

A
  • Signal recognition particle binds to signal sequence, and translation is paused until attaches to SRP receptor in ER membrane
  • Translation continues and translocation begins
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15
Q

What does the N-terminal signal sequence also act as?

A

START-TRANSFER sequence

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16
Q

The start-transfer sequence binds to ___________ and then is discharged into the bilayer once translocation is complete

A

active translocator

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17
Q

Describe the mechanism by which LDL receptor is placed in plasma membrane (4 steps)

A
  • Start transfer sequence opens translocator
  • Stop transfer sequence enters translocator
  • Translocator opens and discharges start transfer sequence laterally

(one pass transmembrane protein)

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18
Q

What three changes occur in ER lumen that lead to formation of the triple helix in collagen?

A

1) signal peptide of N terminus dissolves
2) hydroxylation of lysines and prolines
3) glycosylation (addn of glucose/galactose monomers onto hydroxyl groups) on lysines

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19
Q

Why does lack of Vitamin C cause scurvy?

A

Because Vitamin C is a cofactor in the hydroxylations of lysines and prolines during the formation of the triple helix of collagen therefore collagen triple helices are loose

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20
Q

Does stop transfer sequence stop translation?

A

NO

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21
Q

When a single pass transmembrane protein is inserted into the ER membrane, what determine that the N terminus is on the cytosolic side?

A

If more positively charged AA immediately proceed hydrophobic core of start transfer sequence

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22
Q

How does a multipass transmembrane protein get inserted

A

same process as any transmembrane protein but translocator does not discharge start transfer sequence laterally until FINAL stop transfer sequence has entered

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23
Q

What is the significance of coated vesicles? Name three types

A

Different protein coats select different cargo. COPI, COPII, clathrin

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24
Q

After being processed in the golgi apparatus, what happens to procollagen?

A

It is packaged by COP1 proteins into a secretory vesicle destined for extracellular space

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25
Q

What occurs in the regulated secretory pathway?

A

Selected proteins in TGN are directed into secretory vesicles where proteins are concentrated and stored until extracellular signal stimulates their secretion

26
Q

The human pancreas has the largest capacity for protein synthesis of any organ in human body. What is much of capacity used for?

A

synthesizing digestive enzymes in acinar cells

27
Q

Which of the following enzymes is not stored in pancreas?

a) alpha amylase
b) beta lactamase
c) lipase
d) RNAse
e) DNAse

A

b

28
Q

What is a pancreas consensus element?

A

They are enhancer regions found on genes for digestive enzymes that regulate transcription of mRNAs

29
Q

________, a transcription factor, binds to pancreas consensus elements and essential for __________________

A

PTF-1, expression of digestive enzymes

30
Q

What is the endocrine function of the pancreas?

A

Produce and secrete insulin and glucagon

31
Q

What occurs in exocrine pancreatic insufficiency?

A

Pancreas is damaged and cannot produce enough enzymes to digest food –> fail to get nutrition from food eaten

32
Q

Which of the following is NOT a disease caused by exocrine pancreatic insufficiency?

a) chronic pancreatitis
b) celiac disease
c) crohn’s disease
d) diabetes
e) all of the above are caused by EPI

A

e)

33
Q

in Zollinger Ellison, what causes EPI?

A

acid mediated deactivation of pancreatic enzymes

34
Q

What causes EPI in Celiac disease?

A

Decreased pancreatic stimulation

35
Q

Obstruction of the main pancreatic duct can result in?

A

Tumor

36
Q

What type of transport do clathrin coats mediate?

A

receptor-mediated vesicular transport

37
Q

What do clathrin coated vesicles accomplish in TGN?

A

1) sort lysosomal proteins for transport to lysosomes

2) sort substrances for storage in secretory vesicles

38
Q

What do clathirin coated vesicles accomplish at plasma membrane?

A

Used for uptake of extracellular material via RECEPTOR MEDIATED ENDOCYTOSIS

39
Q

Digestive enzyme exocytosis is stimulated by what?

A

neurohormal agents such as acetylcholine

40
Q

Clathrin coats mediate formation of secretory vesicles also called what?

A

zymogen granules

41
Q

When someone eats, the exocrine pancreas must replenish stores of digestive enzymes. This triggers three processes:

A

1) unfolded protein response - inc synth of chaperones and foldases
2) upregulation of systems involved in degradation of un/mis folded proteins
3) ER-associated protein degradation = required to rid cell of mis/un folded toxic proteins

42
Q

The adaptive unfolded protein response has 3 functions

A

1) inc expression and funcn of chaperones and foldases
2) activate ERAD
3) global reduction in translation of mRNA everywhere ELSE

43
Q

Where does calnexin, the membrane bound chaperone bind to incompletely folded proteins?

A

1 terminal glucose on N-linked oligosaccharide

44
Q

Where are proteins glycosylated ? (location of cell)

A

ER lumen

45
Q

What happens to protein once it is bound by calnexin?

A

It is trapped in the ER to refold, terminal glucose is removed in process. After released, glucose transferase determines if folded properly. if not, glucose added to restart process

46
Q

How are proteins degraded through ERAD?

A

Proteasome

47
Q

Liver is central to the regulation of what?

A

Cholesterol levels - synthesizes for export and removes from body by converting to bile salts

48
Q

Describe LDL cholesterol

A

“bad”, main carrier of cholesterol in circulation, main source of build up and blockage in arteries

49
Q

Describe HDL cholesterol

A

good, helps remove cholesterol from arteries

50
Q

Describe triglycerides

A

Another form of fat in blood that can raise your risk of heart disease

51
Q

What molecule is recognized by LDL receptor for removal of LDL from circulation and delivery of cholesterol to cell?

A

apolipoprotein B10

52
Q

Cholesterol is a precursor for (3)

A

steroid hormones, bile acids, vitamin D

53
Q

Receptor mediated endocytosis of LDL

A

LDL binds to LDL receptor in ER membrane and is endocytosed through clathrin coated pit

54
Q

What type of mutation can lead to hyperchoelesteremia?

A

LDL receptor protein with defective coated pit binding site

55
Q

Familial hypercholesteremia is a ___________ disorder caused by mutations in LDL receptors

A

autosomal dominant

56
Q

Heterozygotes for FH are present in 1 / ______ people whereas homozygotes are 1 / _____ people

A

500, million

57
Q

In homozygotes for FH, sudden death and acute MI may happen as early as ______ years old

A

1-2 years

58
Q

In heterozygotes for FH, CAD in men develops in _____

A

40s - women delayed by 10-15 yrs

59
Q

How is free cholesterol released in bloodstream (start in ER)

A

LDL endocytosed –> vesicle uncoated -> fusion with endosome –> lysosome –> free cholesterol released

60
Q

Lysosomes contain what type of pump

A

ATP driven H+

61
Q

What tag diverts proteins to lysosome

A

mannose 6 phosphate

62
Q

What are the three paths towards lysosomal degradation

A

endocytosis
autophagy
phagocytosis

B1 (18 decks)

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